Our previous study showed in vitro upregulation of TFAP2A 1 day after treatment with cetuximab.12 Together with the fact that some of its targets are receptor tyrosine kinases,14,15 it is very probable that TFAP2A upregulation, or of its targets, is one of the mechanisms activated by HNSCC cells to overcome EGFR blockade and that will induce resistance. This evidence concerns the gene NTRK1 and head and neck squamous cell carcinoma.